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map kinase p44 42  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc map kinase p44 42
    Map Kinase P44 42, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 13441 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/p44+42+map+kinase/p44%2F42+MAPK+(Erk1%2F2)+Antibody/pmc13016477-357-12-15
    Average 99 stars, based on 13441 article reviews
    map kinase p44 42 - by Bioz Stars, 2026-09
    99/100 stars

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    Related Articles

    other:

    Article Title: Diabetic Ketoacidosis Induces Tau Hyperphosphorylation in Rat Brain
    Article Snippet: MAPK (Erk1/2) , Rabbit , 42/44 , Total p44/42 MAP Kinase (Erk1/Erk2) , Cell signaling , 9102.

    Article Title: Pathogen size alters C-type lectin receptor signaling in dendritic cells to influence CD4 Th9 cell differentiation
    Article Snippet: p44/42 MAP kinase (phosphorylated Erk1/2) antibody , Cell Signaling Technology , Cat# 9101; RRID: AB_331646.

    Article Title: Integrin-KCNB1 potassium channel complexes regulate neocortical neuronal development and are implicated in epilepsy
    Article Snippet: p44/42 MAP kinase (phosphorylated Erk1/2) , Cell Signaling Technology , Cat# 9101, RRID:AB_331646.

    Recombinant:

    Article Title: <scp>KCNB1</scp>‐Leptin receptor complexes couple electric and endocrine function in the melanocortin neurons of the hypothalamus
    Article Snippet: .. Reagent or resource Source Identifier Antibodies POMC (D3R1U) Rabbit mAb Cell Signaling Technology #23499 c- Fos (9F6) Rabbit mAb Cell Signaling Technology #2250 Stat3 (124H6) Mouse mAb Cell Signaling Technology #9139 Phospho- Stat3 (Tyr705) (M9C6) Mouse mAb Cell Signaling Technology #4113 FoxO1 (C29H4) Rabbit mAb Cell Signaling Technology #2880 Phospho- FoxO1 (Ser256) (E1F7T) Rabbit mAb Cell Signaling Technology #84192 p44/42 MAP kinase (phosphorylated Erk1/2) Cell Signaling Technology Cat# 9101 p44/42 MAPK (Erk1/2) (137F5) Rabbit mAb Cell Signaling Technology Cat# 4695 Integrin beta- 5 (D24A5) Rabbit mAb Cell Signaling Technology Cat# 3629 Integrin beta- 1 antibody Cell Signaling Technology Cat #4706 Alpha MSH polyclonal rabbit Bioss Antibodies bs- 1848R AgRP polyclonal antibody Thermo Fisher PA5- 118934 Leptin receptor polyclonal antibody Thermo Fisher PA1- 053 Leptin receptor recombinant Rabbit monoclonal antibody Thermo Fisher MA5- 32685 (NIH), Grant/Award Number: R01AG060919; National Science Foundation (NSF), Grant/Award Number: 2030348 upon leptin stimulation. ..

    Article Title: KSR1 mediates small-cell lung carcinoma tumor initiation and cisplatin resistance
    Article Snippet: Small cell lung cancer (SCLC) has a dismal 5-year survival rate of less than 7%, with limited advances in first-line treatment over the past four decades.. Tumor-initiating cells (TIC) contribute to resistance and relapse, a major impediment to SCLC treatment.. In this study, we identify kinase suppressor of Ras 1 (KSR1), a molecular scaffold for the Raf/MEK/ERK signaling cascade, as a critical regulator of SCLC TIC formation and tumor initiation in vivo.

    Plasmid Preparation:

    Article Title: KSR1 mediates small-cell lung carcinoma tumor initiation and cisplatin resistance
    Article Snippet: Small cell lung cancer (SCLC) has a dismal 5-year survival rate of less than 7%, with limited advances in first-line treatment over the past four decades.. Tumor-initiating cells (TIC) contribute to resistance and relapse, a major impediment to SCLC treatment.. In this study, we identify kinase suppressor of Ras 1 (KSR1), a molecular scaffold for the Raf/MEK/ERK signaling cascade, as a critical regulator of SCLC TIC formation and tumor initiation in vivo.

    Construct:

    Article Title: KSR1 mediates small-cell lung carcinoma tumor initiation and cisplatin resistance
    Article Snippet: Small cell lung cancer (SCLC) has a dismal 5-year survival rate of less than 7%, with limited advances in first-line treatment over the past four decades.. Tumor-initiating cells (TIC) contribute to resistance and relapse, a major impediment to SCLC treatment.. In this study, we identify kinase suppressor of Ras 1 (KSR1), a molecular scaffold for the Raf/MEK/ERK signaling cascade, as a critical regulator of SCLC TIC formation and tumor initiation in vivo.

    Retroviral:

    Article Title: KSR1 mediates small-cell lung carcinoma tumor initiation and cisplatin resistance
    Article Snippet: Small cell lung cancer (SCLC) has a dismal 5-year survival rate of less than 7%, with limited advances in first-line treatment over the past four decades.. Tumor-initiating cells (TIC) contribute to resistance and relapse, a major impediment to SCLC treatment.. In this study, we identify kinase suppressor of Ras 1 (KSR1), a molecular scaffold for the Raf/MEK/ERK signaling cascade, as a critical regulator of SCLC TIC formation and tumor initiation in vivo.

    Disruption:

    Article Title: KSR1 mediates small-cell lung carcinoma tumor initiation and cisplatin resistance
    Article Snippet: Small cell lung cancer (SCLC) has a dismal 5-year survival rate of less than 7%, with limited advances in first-line treatment over the past four decades.. Tumor-initiating cells (TIC) contribute to resistance and relapse, a major impediment to SCLC treatment.. In this study, we identify kinase suppressor of Ras 1 (KSR1), a molecular scaffold for the Raf/MEK/ERK signaling cascade, as a critical regulator of SCLC TIC formation and tumor initiation in vivo.



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    Image Search Results


    Effect of introducing point mutations on the biological activity of FGF1. a Serum-starved NIH 3T3 cells were treated with 10 ng/mL FGF1 variants for 15 min in the presence of heparin (10 U/mL). Activation of the downstream cascade was detected by immunoblotting using the following antibodies: anti-phospho-FRS2 (pFRS2) and anti-phospho-ERK1/2 (pERK1/2). Anti-ERK1/2 and anti-vinculin antibodies were used to confirm equal loading. Representative results are shown (n ≥ 3). The vertical lines in the last WB panel show the deleted wells. The original membranes, together with the method of trimming, are presented in Fig. S2. Densitometric analysis of pERK/ERK is presented in Fig. S3. b Effect of 20-h FGF1 variants stimulation (20 ng/mL) in the presence of 10 U/mL heparin on glucose uptake by 3T3-L1 adipocytes. Data are presented as mean ± SEM, n = 4. Statistical significance: * p ≤ 0.05; ** p ≤ 0.01 and *** p ≤ 0.001

    Journal: Molecular Biomedicine

    Article Title: Engineered fibroblast growth factor 1 variants uncouple glucose-lowering effects from mitogenic activity with therapeutic potential for type 2 diabetes

    doi: 10.1186/s43556-025-00398-w

    Figure Lengend Snippet: Effect of introducing point mutations on the biological activity of FGF1. a Serum-starved NIH 3T3 cells were treated with 10 ng/mL FGF1 variants for 15 min in the presence of heparin (10 U/mL). Activation of the downstream cascade was detected by immunoblotting using the following antibodies: anti-phospho-FRS2 (pFRS2) and anti-phospho-ERK1/2 (pERK1/2). Anti-ERK1/2 and anti-vinculin antibodies were used to confirm equal loading. Representative results are shown (n ≥ 3). The vertical lines in the last WB panel show the deleted wells. The original membranes, together with the method of trimming, are presented in Fig. S2. Densitometric analysis of pERK/ERK is presented in Fig. S3. b Effect of 20-h FGF1 variants stimulation (20 ng/mL) in the presence of 10 U/mL heparin on glucose uptake by 3T3-L1 adipocytes. Data are presented as mean ± SEM, n = 4. Statistical significance: * p ≤ 0.05; ** p ≤ 0.01 and *** p ≤ 0.001

    Article Snippet: The following primary antibodies were used: anti-phospho-FGFR (Tyr653/Tyr654) (pFGFR) (#06–1433) from Millipore, anti-tubulin (#T6557) from Sigma-Aldrich, anti-FGFR1 (FGFR1) (#9740), anti-phospho-p44/42 (Thr202/Tyr204) MAP kinase (pERK1/2) (#9101), anti-p44/42 MAP kinase (ERK1/2) (#9102), anti-phospho-FRS2α (Tyr196) (pFRS2) (#3864), anti-vinculin (#13901), anti-phospho-PLCγ1 (Tyr783) (pPLCγ) (#14,008), anti-PLCγ1 (#5690), anti-Glut1 (#73,015) and anti-FGF1 (#3139) from Cell Signaling Technology.

    Techniques: Activity Assay, Activation Assay, Western Blot

    Impaired activation of signaling pathways by FGF1 variants due to reduced affinity for the FGFR1 (IIIc) receptor. a Serum-starved NIH 3T3 cells were stimulated with 10 ng/mL FGF1 variants in the presence of heparin (10 U/mL) for 15 min, and activation of downstream signaling cascades was detected by immunoblotting using the following antibodies: anti-phospho-FGFR (pFGFR), anti-phospho-PLCγ (pPLCγ), anti-phosphoFRS2 (pFRS2), anti-phospho-ERK1/2 (pERK1/2). Anti-ERK1/2, anti-FGFR1, anti-PLCγ and anti-γTubulin antibodies were used to confirm equal loading. Representative results are shown. Densitometric analysis is presented as mean ± SEM, n = 3/4. Statistical significance: * p ≤ 0.05; ** p ≤ 0.01 and *** p ≤ 0.001. b BLI analysis of the affinity of FGF1 variants for FGFR1-Fc (IIIc isoform). FGFR1-Fc was immobilized on a Protein A sensor and its interactions (association and dissociation) with selected FGF1 mutants were analyzed in the concentration range of 100–800 nM. Curves obtained by global fitting are marked in red. Representative results are shown (n ≥ 3). The equilibrium dissociation constant (K D ) was calculated from the saturation binding curve

    Journal: Molecular Biomedicine

    Article Title: Engineered fibroblast growth factor 1 variants uncouple glucose-lowering effects from mitogenic activity with therapeutic potential for type 2 diabetes

    doi: 10.1186/s43556-025-00398-w

    Figure Lengend Snippet: Impaired activation of signaling pathways by FGF1 variants due to reduced affinity for the FGFR1 (IIIc) receptor. a Serum-starved NIH 3T3 cells were stimulated with 10 ng/mL FGF1 variants in the presence of heparin (10 U/mL) for 15 min, and activation of downstream signaling cascades was detected by immunoblotting using the following antibodies: anti-phospho-FGFR (pFGFR), anti-phospho-PLCγ (pPLCγ), anti-phosphoFRS2 (pFRS2), anti-phospho-ERK1/2 (pERK1/2). Anti-ERK1/2, anti-FGFR1, anti-PLCγ and anti-γTubulin antibodies were used to confirm equal loading. Representative results are shown. Densitometric analysis is presented as mean ± SEM, n = 3/4. Statistical significance: * p ≤ 0.05; ** p ≤ 0.01 and *** p ≤ 0.001. b BLI analysis of the affinity of FGF1 variants for FGFR1-Fc (IIIc isoform). FGFR1-Fc was immobilized on a Protein A sensor and its interactions (association and dissociation) with selected FGF1 mutants were analyzed in the concentration range of 100–800 nM. Curves obtained by global fitting are marked in red. Representative results are shown (n ≥ 3). The equilibrium dissociation constant (K D ) was calculated from the saturation binding curve

    Article Snippet: The following primary antibodies were used: anti-phospho-FGFR (Tyr653/Tyr654) (pFGFR) (#06–1433) from Millipore, anti-tubulin (#T6557) from Sigma-Aldrich, anti-FGFR1 (FGFR1) (#9740), anti-phospho-p44/42 (Thr202/Tyr204) MAP kinase (pERK1/2) (#9101), anti-p44/42 MAP kinase (ERK1/2) (#9102), anti-phospho-FRS2α (Tyr196) (pFRS2) (#3864), anti-vinculin (#13901), anti-phospho-PLCγ1 (Tyr783) (pPLCγ) (#14,008), anti-PLCγ1 (#5690), anti-Glut1 (#73,015) and anti-FGF1 (#3139) from Cell Signaling Technology.

    Techniques: Activation Assay, Protein-Protein interactions, Western Blot, Concentration Assay, Binding Assay